Objective：Alzheimer’s disease（AD）is a progressive and irreversible neurodegenerative disorder characterized by pathological features including abnormal β-amyloid（Aβ）deposition，glial hyperactivation，synaptic impairment，and myelin dysfunction. The enriched environment（EE），a non -pharmacological intervention，has garnered attention for its potential to enhance neuroplasticity. However，the effects of EE on social behavior and associated neuropathology during the early stages of AD remain insufficiently explored. This study utilized the 5×FAD mouse model to systematically investigate the impact of EE on early pathological progression in AD，providing new evidence to support the application of EE in the prevention and treatment of AD. Methods：Two-month-old 5 × FAD mice were randomly assigned to a standard environment（SE）group or an EE group（5 mice per cage）and maintained in their respective housing conditions for four weeks. Behavioral tests，including the Y-maze，open field，elevated plus maze，and three-chamber social interaction assays were conducted. Subsequently，immunohistochemistry and Western blot were used to detect the distribution and expression of postsynaptic density protein-95（PSD-95），synaptophysin（SYP）and myelin basic protein （MBP）in the medial prefrontal cortex（mPFC）. Immunofluorescence staining and transmission electron microscopy were combined to observe the changes in neuronal，synaptic structure and myelin morphology to evaluate neuropathological changes. Results：EE did not affect short-term spatial memory or anxiety-like behaviors in 5 × FAD mice but significantly enhanced their social interaction capabilities. Pathologically，5× FAD mice exhibited marked Aβ deposition and glial activation in the mPFC. Compared with the SE group，EE mice showed significantly reduced Aβ accumulation and glial activation in the mPFC. Furthermore，EE improved myelin structural integrity in this region，while no significant effects were observed on synaptic proteins，synaptic ultrastructure，or neuronal survival. Conclusion：EE effectively mitigates AD-related pathology in 5 × FAD mice and alleviates social behavioral deficits， highlighting its potential for addressing AD-associated social dysfunction. These findings suggest that environmental interventions may exert neuroprotective effects by modulating neuroinflammation，reducing Aβ deposition，and preserving myelin homeostasis during AD progression.